Laminar organization of the pyramidal cell layer of the subiculum in the rat

2001 ◽  
Vol 435 (1) ◽  
pp. 89-110 ◽  
Author(s):  
Norio Ishizuka

Neuroreport ◽  
1996 ◽  
Vol 7 (18) ◽  
pp. 3063-3068 ◽  
Author(s):  
Hirohisa Ishimaru ◽  
Koichi Ishikawa ◽  
Seiichi Haga ◽  
Mikio Shoji ◽  
Yoshihide One ◽  
...  


2002 ◽  
Vol 94 (3) ◽  
pp. 655-660 ◽  
Author(s):  
Sihua Qi ◽  
Ren-Zhi Zhan ◽  
Chaoran Wu ◽  
Hideyoshi Fujihara ◽  
Kiichiro Taga ◽  
...  




2002 ◽  
Vol 22 (10) ◽  
pp. 1189-1195 ◽  
Author(s):  
Karen Horsburgh ◽  
I. Mhairi Macrae ◽  
Hilary Carswell

Estrogen can ameliorate brain damage in experimental models of focal cerebral ischemia. In vitro, estrogen increases levels of apolipoprotein E (apoE), which also has neuroprotective effects in brain injury. The authors tested the hypotheses that physiologically relevant levels of 17β-estradiol are neuroprotective in global cerebral ischemia and that neuroprotection is mediated via apoE. In the first study, subcutaneous implants of 17β-estradiol were tested in female C57Bl/6J mice (ovariectomized and nonovariectomized) and plasma levels measured by radioimmunoassay to validate that physiologically relevant levels could be achieved. In the second study, female C57Bl/6J and apoE-deficient mice were ovariectomized and implanted with 17β-estradiol or placebo pellet. Two weeks later, transient global ischemia was induced by bilateral carotid artery occlusion and the mice killed after 72 hours. Ischemic and normal neurons were counted in the caudate nucleus and CA1 pyramidal cell layer and the percentage of neuronal damage was compared between the treated groups. In C57Bl/6J mice, there was less neuronal damage in the 17β-estradiol-treated group compared with placebo group in the caudate nucleus (15 ± 20% versus 39 ± 27%, P = 0.02) and in the CA1 pyramidal cell layer (1.8 ± 2% versus 10 ± 14%, P = 0.08). In contrast, neuronal damage was not significantly different between the 17β-estradiol and placebo groups in apoE-deficient mice in the caudate nucleus (47 ± 35% versus 53 ± 29%, P = 0.7) or in the CA1 pyramidal cell layer (24 ± 19% versus 24 ± 19%, P = 1.0). The data indicate a neuroprotective role for estrogen in global ischemia, the mechanism of which is apoE-dependent.



2004 ◽  
Vol 24 (1) ◽  
pp. 62-66 ◽  
Author(s):  
Thomas H. Gillingwater ◽  
Jane E. Haley ◽  
Richard R. Ribchester ◽  
Karen Horsburgh

The Wlds mouse mutant demonstrates a remarkable phenotype of delayed axonal and synaptic degeneration after nerve lesion. In this study, the authors tested the hypothesis that expression of Wld protein is neuroprotective in an in vivo mouse model of global cerebral ischemia. This model is associated with selective neuronal degeneration in specific brain regions such as the caudate nucleus and CA2 hippocampal pyramidal cell layer. The extent of neuronal damage was quantified in Wlds compared to wild-type mice after an identical episode of global cerebral ischemia. The results demonstrated a significant and marked reduction in the extent of neuronal damage in Wlds as compared to wild-type C57Bl/6 mice. In the caudate nucleus, Wld expression significantly reduced the percentage of ischemic neuronal damage after global ischemia (Wlds, 27.7 ± 16.8%; wild-type mice, 58.7 ± 32.3%; P = 0.036). Similarly, in the CA2 pyramidal cell layer, there was a significant reduction of neuronal damage in the Wlds mice as compared to wild-type mice after ischemia (Wlds, 17.7 ± 23.0%; wild-type mice, 41.9 ± 28.0%; P < 0.023). Thus, these results clearly demonstrate that the Wld gene confers substantial neuroprotection after cerebral ischemia, and suggest a new role to that previously described for Wlds.



1996 ◽  
Vol 206 (2-3) ◽  
pp. 117-120 ◽  
Author(s):  
Toshihiko Kuroiwa ◽  
Masahiro Terakado ◽  
Tokio Yarnaguchi ◽  
Shu Endo ◽  
Masato Ueki ◽  
...  




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